Advanced Trauma Life Support ATLS Student Course Manual 2018
INITIAL PATIENT ASSESSMENT 45 Preload, the volume of venous blood return to the left and right sides of the heart, is determined by venous capacitance, volume status, and the difference between mean venous systemic pressure and right atrial pressure. This pressure differential determines venous flow. The venous system can be considered a reservoir, or capacitance, system in which the volume of blood is divided into two components: 1. The first component represents the volume of blood that would remain in this capacitance circuit if the pressure in the system were zero. This component does not contribute to the mean systemic venous pressure. 2. The second component represents the venous volume that contributes to the mean systemic venous pressure. Nearly 70% of the body’s total blood volume is estimated to be located in the venous circuit. Compliance of the venous system involves a relationship between venous volume and venous pressure. This pressure gradient drives venous flow and therefore the volume of venous return to the heart. Blood loss depletes this component of venous volume and reduces the pressure gradient; consequently, venous return is reduced. The volume of venous blood returned to the heart determines myocardial muscle fiber length after ventricular filling at the end of diastole. According to Starling’s law, muscle fiber length is related to the contractile properties of myocardial muscle. Myocardial contractility is the pump that drives the system. Afterload, also known as peripheral vascular resistance, is systemic. Simply stated, afterload is resistance to the forward flow of blood. Blood Loss Pathophysiology Early circulatory responses to blood loss are compensatory and include progressive vasoconstriction of cutaneous, muscular, and visceral circulation to preserve blood flow to the kidneys, heart, and brain. The usual response to acute circulating volume depletion is an increase in heart rate in an attempt to preserve cardiac output. In most cases, tachycardia is the earliest measurable circulatory sign of shock. The release of endogenous catecholamines increases peripheral vascular resistance, which in turn increases diastolic blood pressure and reduces pulse pressure. However, this increase in pressure does little to increase organ perfusion and tissue oxygenation. For patients in early hemorrhagic shock, venous return is preserved to some degree by the compensatory mechanism of contraction of the volume of blood in the venous system. This compensatory mechanism is limited. The most effective method of restoring adequate cardiac output, end-organ perfusion, and tissue oxygenation is to restore venous return to normal by locating and stopping the source of bleeding. Volume repletion will allow recovery from the shock state only when the bleeding has stopped. At the cellular level, inadequately perfused and poorly oxygenated cells are deprived of essential substrates for normal aerobic metabolism and energy production. Initially, compensation occurs by shifting to anaerobic metabolism, resulting in the formation of lactic acid and development of metabolic acidosis. If shock is prolonged, subsequent end-organ damage and multiple organ dysfunction may result. Administration of an appropriate quantity of isotonic electrolyte solutions, blood, and blood products helps combat this process. Treatment must focus on reversing the shock state by stopping the bleeding and providing adequate oxygenation, ventilation, and appropriate fluid resuscitation. Rapid intravenous access must be obtained. Definitive control of hemorrhage and restoration of adequate circulating volume are the goals of treating hemorrhagic shock. Vasopressors are contraindicated as a first-line treatment of hemorrhagic shock because they worsen tissue perfusion. Frequently monitor the patient’s indices of perfusion to detect any deterioration in the patient’s condition as early as possible so it can be reversed. Monitoring also allows for evaluation of the patient’s response to therapy. Reassessment helps clinicians identify patients in compensated shock and those who are unable to mount a compensatory response before cardiovascular collapse occurs. Most injured patients who are in hemorrhagic shock require early surgical intervention or angioembolization to reverse the shock state. The presence of shock in a trauma patient warrants the immediate involvement of a surgeon. Strongly consider arranging for early transfer of these patients to a trauma center when they present to hospitals that are not equipped to manage their injuries. Initial Patient Assessment Optimally, clinicians recognize the shock state during the initial patient assessment. To do so, they must be familiar with the clinical differentiation of causes of shock—chiefly, hemorrhagic and non-hemorrhagic shock. n BACK TO TABLE OF CONTENTS
46 CHAPTER 3 n Shock Recognition of Shock Profound circulatory shock, as evidenced by hemodynamic collapse with inadequate perfusion of the skin, kidneys, and central nervous system, is simple to recognize. After ensuring a patent airway and adequate ventilation, trauma team members must carefully evaluate the patient’s circulatory status for early manifestations of shock, such as tachycardia and cutaneous vasoconstriction. Relying solely on systolic blood pressure as an indicator of shock can delay recognition of the condition, as compensatory mechanisms can prevent a measurable fall in systolic pressure until up to 30% of the patient’s blood volume is lost. Look closely at pulse rate, pulse character, respiratory rate, skin perfusion, and pulse pressure (i.e., the difference between systolic and diastolic pressure). In most adults, tachycardia and cutaneous vasoconstriction are the typical early physiologic responses to volume loss. Any injured patient who is cool to the touch and is tachycardic should be considered to be in shock until proven otherwise. Occasionally, a normal heart rate or even bradycardia is associated with an acute reduction of blood volume; other indices of perfusion must be monitored in these situations. The normal heart rate varies with age. Tachycardia is diagnosed when the heart rate is greater than 160 beats per minute (BPM) in an infant, 140 BPM in a preschool-aged child, 120 BPM in children from school age to puberty, and 100 BPM in adults. Elderly patients may not exhibit tachycardia because of their limited cardiac response to catecholamine stimulation or the concurrent use of medications, such as ß-adrenergic blocking agents. The body’s ability to increase the heart rate also may be limited by the presence of a pacemaker. A narrowed pulse pressure suggests significant blood loss and involvement of compensatory mechanisms. Massive blood loss may produce only a slight decrease in initial hematocrit or hemoglobin concentration. Thus, a very low hematocrit value obtained shortly after injury suggests either massive blood loss or a preexisting anemia, and a normal hematocrit does not exclude significant blood loss. Base deficit and/or lactate levels can be useful in determining the presence and severity of shock. Serial measurements of these parameters to monitor a patient’s response to therapy are useful. organ perfusion and tissue oxygenation due to poor cardiac performance from blunt myocardial injury, cardiac tamponade, or a tension pneumothorax that produces inadequate venous return (preload). To recognize and manage all forms of shock, clinicians must maintain a high level of suspicion and carefully observe the patient’s response to initial treatment. Initial determination of the cause of shock requires an appropriate patient history and expeditious, careful physical examination. Selected additional tests, such as chest and pelvic x-rays and focused assessment with sonography for trauma (FAST) examinations, can confirm the cause of shock, but should not delay appropriate resuscitation. (See FAST video on MyATLS mobile app.) Overview of Hemorrhagic Shock Hemorrhage is the most common cause of shock after injury, and virtually all patients with multiple injuries have some degree of hypovolemia. Therefore, if signs of shock are present, treatment typically is instituted as if the patient were hypovolemic. However, while instituting treatment, it is important to identify the small number of patients whose shock has a different cause (e.g., a secondary condition, such as cardiac tamponade, tension pneumothorax, spinal cord injury, or blunt cardiac injury), which complicates the presentation of hemorrhagic shock. The treatment of hemorrhagic shock is described later in this chapter, but the primary focus is to promptly identify and stop hemorrhage. Sources of potential blood loss—chest, abdomen, pelvis, retroperitoneum, extremities, and external bleeding—must be quickly assessed by physical examination and appropriate adjunctive studies. Chest x-ray, pelvic x-ray, abdominal Clinical Differentiation of Cause of Shock Shock in a trauma patient is classified as hemorrhagic or non-hemorrhagic shock. A patient with injuries above the diaphragm may have evidence of inadequate n FIGURE 3-2 Using ultrasound (FAST) to search for the cause of shock. n BACK TO TABLE OF CONTENTS
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INITIAL PATIENT ASSESSMENT 45<br />
Preload, the volume of venous blood return to the<br />
left and right sides of the heart, is determined by<br />
venous capacitance, volume status, and the difference<br />
between mean venous systemic pressure and right atrial<br />
pressure. This pressure differential determines venous<br />
flow. The venous system can be considered a reservoir,<br />
or capacitance, system in which the volume of blood is<br />
divided into two components:<br />
1. The first component represents the volume of<br />
blood that would remain in this capacitance<br />
circuit if the pressure in the system were zero.<br />
This component does not contribute to the mean<br />
systemic venous pressure.<br />
2. The second component represents the venous<br />
volume that contributes to the mean systemic<br />
venous pressure. Nearly 70% of the body’s total<br />
blood volume is estimated to be located in the<br />
venous circuit. Compliance of the venous system<br />
involves a relationship between venous volume<br />
and venous pressure. This pressure gradient<br />
drives venous flow and therefore the volume of<br />
venous return to the heart. Blood loss depletes<br />
this component of venous volume and reduces<br />
the pressure gradient; consequently, venous<br />
return is reduced.<br />
The volume of venous blood returned to the heart<br />
determines myocardial muscle fiber length after<br />
ventricular filling at the end of diastole. According<br />
to Starling’s law, muscle fiber length is related to<br />
the contractile properties of myocardial muscle.<br />
Myocardial contractility is the pump that drives<br />
the system.<br />
Afterload, also known as peripheral vascular resistance,<br />
is systemic. Simply stated, afterload is resistance<br />
to the forward flow of blood.<br />
Blood Loss Pathophysiology<br />
Early circulatory responses to blood loss are compensatory<br />
and include progressive vasoconstriction<br />
of cutaneous, muscular, and visceral circulation<br />
to preserve blood flow to the kidneys, heart, and<br />
brain. The usual response to acute circulating<br />
volume depletion is an increase in heart rate in an<br />
attempt to preserve cardiac output. In most cases,<br />
tachycardia is the earliest measurable circulatory sign<br />
of shock. The release of endogenous catecholamines<br />
increases peripheral vascular resistance, which<br />
in turn increases diastolic blood pressure and<br />
reduces pulse pressure. However, this increase in<br />
pressure does little to increase organ perfusion and<br />
tissue oxygenation.<br />
For patients in early hemorrhagic shock, venous<br />
return is preserved to some degree by the compensatory<br />
mechanism of contraction of the volume of blood in<br />
the venous system. This compensatory mechanism<br />
is limited. The most effective method of restoring<br />
adequate cardiac output, end-organ perfusion, and<br />
tissue oxygenation is to restore venous return to normal<br />
by locating and stopping the source of bleeding. Volume<br />
repletion will allow recovery from the shock state only<br />
when the bleeding has stopped.<br />
At the cellular level, inadequately perfused and poorly<br />
oxygenated cells are deprived of essential substrates<br />
for normal aerobic metabolism and energy production.<br />
Initially, compensation occurs by shifting to anaerobic<br />
metabolism, resulting in the formation of lactic acid<br />
and development of metabolic acidosis. If shock is<br />
prolonged, subsequent end-organ damage and multiple<br />
organ dysfunction may result.<br />
Administration of an appropriate quantity of isotonic<br />
electrolyte solutions, blood, and blood products helps<br />
combat this process. Treatment must focus on reversing<br />
the shock state by stopping the bleeding and providing<br />
adequate oxygenation, ventilation, and appropriate<br />
fluid resuscitation. Rapid intravenous access must<br />
be obtained.<br />
Definitive control of hemorrhage and restoration of<br />
adequate circulating volume are the goals of treating<br />
hemorrhagic shock. Vasopressors are contraindicated<br />
as a first-line treatment of hemorrhagic shock because<br />
they worsen tissue perfusion. Frequently monitor<br />
the patient’s indices of perfusion to detect any<br />
deterioration in the patient’s condition as early as<br />
possible so it can be reversed. Monitoring also allows<br />
for evaluation of the patient’s response to therapy.<br />
Reassessment helps clinicians identify patients in<br />
compensated shock and those who are unable to<br />
mount a compensatory response before cardiovascular<br />
collapse occurs.<br />
Most injured patients who are in hemorrhagic shock<br />
require early surgical intervention or angioembolization<br />
to reverse the shock state. The presence of shock in a<br />
trauma patient warrants the immediate involvement<br />
of a surgeon. Strongly consider arranging for early<br />
transfer of these patients to a trauma center when they<br />
present to hospitals that are not equipped to manage<br />
their injuries.<br />
Initial Patient Assessment<br />
Optimally, clinicians recognize the shock state during<br />
the initial patient assessment. To do so, they must be<br />
familiar with the clinical differentiation of causes of<br />
shock—chiefly, hemorrhagic and non-hemorrhagic shock.<br />
n BACK TO TABLE OF CONTENTS